Weak Points Midterm Flashcards

1
Q

Incubation

A

Pathogen replicates no symptoms rapid or slow onset

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2
Q

Prodromal

A

Symptoms become detectable

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3
Q

Acute

A

Tissue damage inflm dt toxins from pathogens being released at lysis. Most severe symptoms

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4
Q

Convalescent

A

Body continues to rid pathogen inf plateaus symptoms decrease

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5
Q

Resolution

A

Pathogen absolutely eliminated no present symptoms

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6
Q

Dysplasia

A

Diff shape size arrangement cells. Faulty tissue. Can progress to anaplasia. Increased mitosis index. Pre cancerous

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7
Q

Necrosis

A

Cell death dt injury. Abnormal. Initiates inflammatory response.

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8
Q

Fibrinous exudate

A

Lots of fibrinogen and other components. Sticky mesh

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9
Q

Membranous exudate

A

Dev of mucous membrane. Necrotic cells in fibropurulent exudate

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10
Q

CRP

A

Hepatic protein produced in response to inflm. Serum marker. Has a role via complement. Increased levels in atherosclerosis

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11
Q

NSAIDS for tx of inflm

A

Decreases prostaglandin synthesis which decreases pain

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12
Q

Steroidal anti inflammatory for tx inflm

A

Decrease cap perm, decrease wbc and mast cells to site, decrease prostaglandin and histamine release

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13
Q

Shock is

A

Acute hypoperfusion leading to hypoxia

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14
Q

Anaphylactic shock

A

Dt severe allergic reaction. Systemic edema dt increased perm. Fluid lost from blood to tissues = hypovolemia = circulatory failure

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15
Q

Mediators released by mast cells during anaphylaxis do what

A

Work on SM of bvs and resp tract. Cause vasoconstriction of resp tract = broncho spasm

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16
Q

Septic shock dt

A

Severe infection. Becomes systemic dt multiple infections and many mediators being released and circulating throughout body.

Vasodilatory = hypotension = hypoperfusion = shock

Causes systemic inflm and multiple organ dysfx

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17
Q

Aneurysms caused by

A

Degenerative change in BV wall (congenital defects, trauma, atherosclerosis) causing localized dilation of an artery

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18
Q

Common sites for aneurysms

A

Abd/thoracic aorta, femoral artery, Iliad and popliteal

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19
Q

Saccular
Fusiform
Dissecting

A

1 sided
Entire circumference
Blood flows Btwn 2 layers bulge

20
Q

Complications of aneurysms

A

Pressure to surrounding
Rupture hemmorhagging
Clotting - thrombosis = distal emboli satin

21
Q

Tx of angina

A

Decreased activity, nitroglycerin

22
Q

When is nitro used

A

Tx of angina, not used DURING AN MI, but used post MI to prevent risk of having another

23
Q

If unstable plaque ruptured

A

Thrombosis- platelets aggregate - PG release - vasopasm

24
Q

Stable angina causes what kind of pain

25
Variant/vasopastic angina
Not caused by atherosclerosis but a thrombus. Happens at rest nocturnally. No known cause. Dt spasm of coronary artery
26
2 types of MI
Subendocardial (Inner 1/3-1/2 v wall. Distal occlusion in coronary branches) Transmural (Entire v wall. 1 proximal artery occluded)
27
DX of mi
ECG abnormalities (ST seg, T wave inversion) Myoglobin CKMB (cardiac muscle specific ez) Troponin I & T (elevates first)
28
Meds to tx mi
Thrombolytics (break up clot, pieces circulate) Antiarrythmics (bring rhythm back that was lost dt met acidosis) Anticoagulants (prevents platelet aggregation, clot can not grow)
29
Cardiomyopathy
Cardiac muscle disorder
30
Hypertrophic cardiomyopathy
Excessive hyper trophy of CM in v wall. Inc wall thickness dec chamber size dec vol into chamber Thick IV septum
31
Hyp. Cardiomyopathy et
50% autosomal dominant (genetic) 50% idiopathic
32
Symptoms of hyp cardiomyopathy if they occur are Tx
Dyspnea, angina, syncope, palpitations, sudden death Negative inotropes, alcohol septal ablation
33
Dilated/congestive cardiomyopathy
V wall enlargement (heart walls stretched) Weak contraction Decreased stroke volume Alcohol abuse implicated
34
Restricted cardiomyopathy
Rigid v walls. Muscle cannot contract or relax, incomplete filling - dec CO. Leads to CHF
35
Arrhythmia occur in only diseases hearts. t or f
F Also in normal hearts
36
Et of arrhythmias
Heart defects, ischemia, mi, drugs, fluid/electrolyte imbalance (effects resting membrane potential), acid base imbalance
37
Atrial flutter
Reg rhythm, increased rate. Atrial tachycardia 300 Bpm. Ventricles tachy 150. A:v 2:1
38
Atrial fibrillation
Spontaneous episode of irregular chaotic contractions 400-600 Bpm. ventricles irregular and rapid 80-180
39
Heart block
Atria fill and empty properly, but conduction of impulses from a to v abn or absent
40
Degrees of heart block
1st: delayed connection. Reg rhythm. Impulse passed but delayed 2nd: some signals conducted, some not. Intermittent failure of conduction 3rd: no conduction Btwn a and v. Nodal cells in v create new pacemaker. A and v have separate rhythms.
41
Ventricular fibrillation
Quivering of v. No cont. can cause death in minutes
42
Tx of arrhythmias
Based on type and if needed. Drugs Defibrillation (clears all electrical activity in heart to reinstate normal sinus rhythm) Sx (ablation of infarcts area that is causing arrhythmia, or pacemaker)
43
Valvular disease et
Age (degenerative change), valve trauma (inf) ischemic change, congenital defects
44
Damage to valves causes either
Stenosis: stiff valve, narrow orifice, flow impeded Incompetence: distorted valves. Improper closure. Regurgitation
45
Tx of valvular disease
Goal to maintain improve fx valves to prevent failure Sx replacement
46
5 steps in disease course
``` Incubation Prodromal Acute Convalescent Resolution ```